Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression: a review (2026)
- Authors:
- USP affiliated authors: BRITTO, LUIZ ROBERTO GIORGETTI DE - ICB ; FERREIRA, ANA FLAVIA FERNANDES - ICB
- Unidade: ICB
- DOI: 10.1016/j.neuint.2025.106091
- Subjects: FISIOLOGIA; DOENÇA DE PARKINSON; DOENÇAS NEURODEGENERATIVAS; CANAIS DE POTÁSSIO; ESTRESSE OXIDATIVO; RECEPTORES DE DOPAMINA
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Neurochemistry International
- ISSN: 1872-9754
- Volume/Número/Paginação/Ano: v. 192, art. 106091, 2026
- Status:
- Artigo aberto em periódico híbrido (Hybrid Open Access)
- Versão do Documento:
- Versão publicada (Published version)
- Acessar versão aberta:
-
ABNT
GUNDI, Barbara et al. Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression: a review. Neurochemistry International, v. 192, 2026Tradução . . Disponível em: https://doi.org/10.1016/j.neuint.2025.106091. Acesso em: 31 mar. 2026. -
APA
Gundi, B., Ho, H. L., Zhang, X., He, A., Xin, D., Ferreira, A. F. F., et al. (2026). Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression: a review. Neurochemistry International, 192. doi:10.1016/j.neuint.2025.106091 -
NLM
Gundi B, Ho HL, Zhang X, He A, Xin D, Ferreira AFF, Feng Z-P, Sun H-S, Britto LRG de. Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression: a review [Internet]. Neurochemistry International. 2026 ; 192[citado 2026 mar. 31 ] Available from: https://doi.org/10.1016/j.neuint.2025.106091 -
Vancouver
Gundi B, Ho HL, Zhang X, He A, Xin D, Ferreira AFF, Feng Z-P, Sun H-S, Britto LRG de. Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression: a review [Internet]. Neurochemistry International. 2026 ; 192[citado 2026 mar. 31 ] Available from: https://doi.org/10.1016/j.neuint.2025.106091 - Inhibition of neuroinflammation by GIBH-130 (AD-16) reduces neurodegeneration, motor deficits, and proinflammatory cytokines in a hemiparkinsonian model
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